19 research outputs found
Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis.
Molecular, genetic and pathological evidence suggests that deficits in GABAergic parvalbumin-positive interneurons contribute to schizophrenia pathophysiology through alterations in the brain's excitation-inhibition balance that result in impaired behaviour and cognition. Although the factors that trigger these deficits are diverse, there is increasing evidence that they converge on a common pathological hub that involves NMDA receptor hypofunction and oxidative stress. These factors have been separately linked to schizophrenia pathogenesis, but evidence now suggests that they are mechanistically interdependent and contribute to a common schizophrenia-associated pathology
Ventricular Slices of Adult Mouse Hearts - a new Multicellular In Vitro Model for Electrophysiological Studies
Inhibitory effects of palmitoylcarnitine and lysophosphatidylcholine on the sodium current of cardiac ventricular cells
Lysophosphatidylcholine Augments Ca<sub>v</sub>3.2 but Not Ca<sub>v</sub>3.1 T-Type Ca<sup>2+</sup> Channel Current Expressed in HEK-293 Cells
Differential effects of lysophospholipids on exocytosis in rat PC12 cells
10.1007/s00702-009-0355-1Journal of Neural Transmission1173301-308JNTR